Introduction: There are many genetic mutations involved in B-cell lymphomagenesis. These mutations contribute to the prognosis of B-cell lymphomas and can be used for and targeted for intervention.
Areas Covered: This review provides an overview of targeted gene therapies for B-cell lymphoma that were newly approved or are under clinical development. These include, TP53 mutations and related pathways, such as BTK inhibitors, MDM2/4 inhibitors, and XPO1 inhibitors; new drugs targeting mutations through competitive inhibition, such as tazemetostat and GSK126; BCL-2-targeted therapeutics, including venetoclax and ABT-263; BTK, IRAK 1/4, HCK, and myddosome complex that targets the MYD88 mutation and the related pathways. In addition, we have also discussed gene mutations that have been reported as potential therapeutic targets, such as TNFAIP3, CARD11.
Expert Opinion: The mechanisms underlying the role of several genetic mutations in lymphomagenesis have been reported, and several studies have designed and developed drugs targeting these mutations. Many of these drugs have been approved for clinical use, while several are still under clinical development. Recent studies have identified additional genetic mutations and gene targets for BCL-2 treatment; however, effective molecular interventions targeting these new targets are yet to be developed.
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http://dx.doi.org/10.1080/17474086.2021.1856652 | DOI Listing |
Cureus
December 2024
Pulmonology and Critical Care, Marshall University Joan C. Edwards School of Medicine, Huntington, USA.
Malignant hyperthermia is a pharmacogenetic disorder that manifests clinically as a hypermetabolic crisis when a patient with a mutation in the ryanodine or dihydropyridine receptor genes is exposed to neuromuscular blocking agents. Depolarizing neuromuscular agents are known to cause malignant hyperthermia, but cases caused by nondepolarizing agents are rarely reported. We present a case consistent with malignant hyperthermia after receipt of cisatracurium, a nondepolarizing anesthetic agent.
View Article and Find Full Text PDFBiochem Biophys Rep
September 2024
Chongqing Engineering Research Center of Medical Electronics and Information Technology, School of Bioinformatics, Chongqing University of Posts and Telecommunications, 400065, Chongqing, PR China.
Our study focused on specific ChR2 variants, particularly those with the Step function Opsins (SFO) mutation at the D156-C128 gate. These are widely used in optogenetics due to their heightened sensitivity to light and bi-stable prolonged activation. However, in some ChR2 variants, specifically D156 mutants, a tail current occurs when continuous light exposure is stopped.
View Article and Find Full Text PDFJACS Au
January 2025
Program in Chemical Biology, Department of Chemical Physiology and Biochemistry, Proteomics Shared Resources, Knight Cancer Institute, Department of Neurology, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, Portland, Oregon 97239, United States.
Proteins regulate biological functions through the formation of distinct protein complexes. Identification and characterization of these protein-protein interactions are critical to deciphering their mechanism of action. Different antibody-based or cross-linking-based methods have been developed to identify the protein-protein interactions.
View Article and Find Full Text PDFJACS Au
January 2025
Department of Chemistry and Industrial Chemistry, University of Pisa, 56124 Pisa, Italy.
Naturally occurring photoenzymes are rare in nature, but among them, fatty acid photodecarboxylases derived from (FAPs) have emerged as promising photobiocatalysts capable of performing the redox-neutral, light-induced decarboxylation of free fatty acids (FAs) into C1-shortened alka(e)nes. Using a hybrid QM/MM approach combined with a polarizable embedding scheme, we identify the structural changes of the active site and determine the energetic landscape of the forward electron transfer (fET) from the FA substrate to the excited flavin adenine dinucleotide. We obtain a charge-transfer diradical structure where a water molecule rearranges spontaneously to form a H-bond interaction with the excited flavin, while the FA's carboxylate group twists and migrates away from it.
View Article and Find Full Text PDFExtracell Vesicle
December 2024
The Jared Grantham Kidney Institute at the University of Kansas Medical Center, Department of Nephrology and Hypertension, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Autosomal dominant polycystic kidney (ADPKD) disease is the commonest genetic cause of kidney failure (affecting 1:800 individuals) and is due to heterozygous germline mutations in either of two genes, and . Homozygous germline mutations in are responsible for autosomal recessive polycystic kidney (ARPKD) disease a rare (1:20,000) but severe neonatal disease. The products of these three genes, (polycystin-1 (PC1 4302(3)aa)), (polycystin-2 (PC2 968aa)) and (fibrocystin (4074aa)) are all present on extracellular vesicles (EVs) termed, PKD-exosome-like vesicles (PKD-ELVs).
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